Rheumatoid arthritis pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
[[Rheumatoid arthritis]] is mediated by the combination of a predisposing genotype upon which genetic factors, environmental and microorganism also contribute | [[Rheumatoid arthritis]] is mediated by the combination of a predisposing genotype upon which genetic factors, environmental and microorganism also contribute resulting in the inflammatory and destruction of the synovial membrane. | ||
'''Environmental factors''': It causes repeated activation of innate immunity at mucosal surfaces. | '''Environmental factors''': It causes repeated activation of innate immunity at mucosal surfaces. | ||
*Smoking interacts with genes to increase susceptibility up to 20- to 40-fold. | *Smoking interacts with genes to increase susceptibility up to 20- to 40-fold. | ||
**Smoking causes increased expression of peptidyl arginine deiminase (PAD) in alveolar macrophages. | **Smoking causes increased expression of peptidyl arginine deiminase (PAD) in alveolar macrophages. | ||
**Peptidyl arginine deiminase convert arginine to citrulline called as citrullination in the airway which further creates neoantigens that can be recognized by the adaptive immune system.<ref name="pmid19479873">{{cite journal |vauthors=Lundström E, Källberg H, Alfredsson L, Klareskog L, Padyukov L |title=Gene-environment interaction between the DRB1 shared epitope and smoking in the risk of anti-citrullinated protein antibody-positive rheumatoid arthritis: all alleles are important |journal=Arthritis Rheum. |volume=60 |issue=6 |pages=1597–603 |date=June 2009 |pmid=19479873 |pmc=2732897 |doi=10.1002/art.24572 |url=}}</ref> | **Peptidyl arginine deiminase convert arginine to citrulline called as citrullination in the airway which further creates neoantigens that can be recognized by the adaptive immune system.<ref name="pmid19479873">{{cite journal |vauthors=Lundström E, Källberg H, Alfredsson L, Klareskog L, Padyukov L |title=Gene-environment interaction between the DRB1 shared epitope and smoking in the risk of anti-citrullinated protein antibody-positive rheumatoid arthritis: all alleles are important |journal=Arthritis Rheum. |volume=60 |issue=6 |pages=1597–603 |date=June 2009 |pmid=19479873 |pmc=2732897 |doi=10.1002/art.24572 |url=}}</ref><ref name="pmid18413445">{{cite journal |vauthors=Makrygiannakis D, Hermansson M, Ulfgren AK, Nicholas AP, Zendman AJ, Eklund A, Grunewald J, Skold CM, Klareskog L, Catrina AI |title=Smoking increases peptidyl arginine deiminase 2 enzyme expression in human lungs and increases citrullination in BAL cells |journal=Ann. Rheum. Dis. |volume=67 |issue=10 |pages=1488–92 |date=October 2008 |pmid=18413445 |doi=10.1136/ard.2007.075192 |url=}}</ref> | ||
'''Microrganism:''' | '''Microrganism:''' | ||
*In periodontal disease, P. gingivalis is | *In periodontal disease, P. gingivalis is commonly found, it also expresses peptidyl arginine deiminases. | ||
*This can lead to citrullination and thereby promote ACPA. | *This can lead to citrullination and thereby promote ACPA. | ||
*A. actinomycetemcomitans produces a toxin that increases calcium influx into neutrophils which further lead to citrullination of peptides and promote APCA. | *A. actinomycetemcomitans produces a toxin that increases calcium influx into neutrophils which further lead to citrullination of peptides and promote APCA. | ||
'''Genetic factors:''' | '''Genetic factors:''' | ||
*Genetics factors like | *Genetics factors like class II major histocompatibility complex (MHC), most common human leukocyte antigen (HLA)-DR. | ||
==Genetics== | ==Genetics== | ||
*[Disease name] is transmitted in [mode of genetic transmission] pattern. | *[Disease name] is transmitted in [mode of genetic transmission] pattern. | ||
Revision as of 17:17, 23 March 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Manpreet Kaur, MD [2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
Rheumatoid arthritis is mediated by the combination of a predisposing genotype upon which genetic factors, environmental and microorganism also contribute resulting in the inflammatory and destruction of the synovial membrane.
Environmental factors: It causes repeated activation of innate immunity at mucosal surfaces.
- Smoking interacts with genes to increase susceptibility up to 20- to 40-fold.
Microrganism:
- In periodontal disease, P. gingivalis is commonly found, it also expresses peptidyl arginine deiminases.
- This can lead to citrullination and thereby promote ACPA.
- A. actinomycetemcomitans produces a toxin that increases calcium influx into neutrophils which further lead to citrullination of peptides and promote APCA.
Genetic factors:
- Genetics factors like class II major histocompatibility complex (MHC), most common human leukocyte antigen (HLA)-DR.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Lundström E, Källberg H, Alfredsson L, Klareskog L, Padyukov L (June 2009). "Gene-environment interaction between the DRB1 shared epitope and smoking in the risk of anti-citrullinated protein antibody-positive rheumatoid arthritis: all alleles are important". Arthritis Rheum. 60 (6): 1597–603. doi:10.1002/art.24572. PMC 2732897. PMID 19479873.
- ↑ Makrygiannakis D, Hermansson M, Ulfgren AK, Nicholas AP, Zendman AJ, Eklund A, Grunewald J, Skold CM, Klareskog L, Catrina AI (October 2008). "Smoking increases peptidyl arginine deiminase 2 enzyme expression in human lungs and increases citrullination in BAL cells". Ann. Rheum. Dis. 67 (10): 1488–92. doi:10.1136/ard.2007.075192. PMID 18413445.